R. Fijnheer (Rob)http://repub.eur.nl/ppl/27716/
List of Publicationsenhttp://repub.eur.nl/eur_signature.pnghttp://repub.eur.nl/
RePub, Erasmus University RepositorySplenectomy for the treatment of thrombotic thrombocytopenic purpurahttp://repub.eur.nl/pub/63563/
Thu, 01 Sep 2005 00:00:01 GMT<div>M.C. Kappers-Klunne</div><div>P.W. Wijermans</div><div>R. Fijnheer</div><div>A.J. Croockewit</div><div>B. van der Holt</div><div>J.T.M. de Wolf</div><div>B. Löwenberg</div><div>A. Brand</div>
Plasma exchange is the treatment of choice for patients with thrombotic thrombocytopenic purpura (TTP) and results in remission in >80% of the cases. Treatment of patients who are refractory to plasma therapy or have relapsing disease is difficult. Splenectomy has been a therapeutic option in these conditions but its value remains controversial. We report on a series of 33 patients with TTP who were splenectomised because they were plasma refractory (n = 9) or for relapsed disease (n = 24). Splenectomy generated prompt and unmaintained remissions in all except five patients, in whom remission was delayed (n = 4) or who died with progressive disease (n = 1). Four postoperative complications occurred: one pulmonary embolism and three surgical complications. Median follow-up after splenectomy was 109 months (range 28-230 months). The overall postsplenectomy relapse rate was 0·09 relapses/patient-year and the 10-year relapse-free survival (RFS) was 70% (95% CI 50-83%). In the patients with relapsing TTP, relapse rate fell from 0·74 relapses/patient-year before splenectomy to 0·10 after splenectomy (P < 0·00001). Two patients died from first postsplenectomy relapse. Although these results are based on retrospective data and that the relapse rate may spontaneously decrease with time, we conclude that splenectomy, when performed during stable disease, has an acceptable safety profile and should be considered in cases of plasma refractoriness or relapsing TTP to reach durable remissions and to reduce or prevent future relapses.Thrombophilias and recurrent pregnancy loss: A critical appraisal of the literaturehttp://repub.eur.nl/pub/71511/
Tue, 01 Feb 2005 00:00:01 GMT<div>I. Krabbendam</div><div>A. Franx</div><div>M.L. Bots</div><div>R. Fijnheer</div><div>H.W. Bruinse</div>
Thrombophilias are suggested to play a role in recurrent miscarriage. The aim of this study was to evaluate the literature of the past 10 years regarding the association between thrombophilias and recurrent miscarriage. We concluded that there is a large variety in applied study methodology. Therefore, we defined criteria for an adequate study on the relationship of thrombophilias on recurrent pregnancy loss: (i) no exclusion criteria for patients or at least the same criteria for patients and controls; (ii) a clear definition of the gestational age at previous losses; (iii) a well-described control group; (iv) clear description of the test methods and moment of testing; and (v) a clear description of the (non) significant differences or odds ratio between cases and controls. Eleven out of 69 studies fulfilled these criteria. Their results show significant higher serum homocysteine levels among women with a history of recurrent miscarriage. No relation was found between recurrent miscarriage and the methylenetetrahydrofolate reductase C667T mutation. No relation was observed for the levels of antithrombin, protein C and protein S. Seven studies on the association of factor V Leiden (FVL) and/or pathologic activated protein C ratio (pAPCR) showed that FVL may play a role in second trimester losses, as do antiphospholipid antibodies. Studies on the prothrombin gene mutation yielded conflicting results. Consequently, large prospective studies according to the aforementioned criteria are needed to establish if there is a relationship between thrombophilias and recurrent miscarriage at all. At present, there is only justification for testing for homocysteine levels, antiphospholipid antibodies and FVL in women with a history of recurrent miscarriage.Spinal dural arteriovenous fistulas are not associated with prothrombotic factorshttp://repub.eur.nl/pub/22487/
Wed, 01 Sep 2004 00:00:01 GMT<div>K. Jellema</div><div>C.C. Tijssen</div><div>R. Fijnheer</div><div>P.G. de Groot</div><div>P.J. Koudstaal</div><div>J. van Gijn</div>
BACKGROUND AND PURPOSE: The cause of spinal dural arteriovenous fistulas (SDAVF) is unknown. In intracranial dural arteriovenous fistulas, an association with factor V Leiden mutation has been found. Therefore, we studied the association between prothrombotic factors and SDAVF.
METHODS: Factor V Leiden mutation, factor II mutation, protein S, protein C, factor VIII, von Willebrand factor, antithrombin III, and lupus anticoagulant were determined by means of standard laboratory tests in 40 patients and 119 control subjects matched for sex and age.
RESULTS: Factor V Leiden mutation was not found in the patient group and was found twice in the control group. Factor II mutation was found in 1 patient and in none of the control subjects. There was no decreased activity of protein S, protein C, factor VIII, von Willebrand factor, or antithrombin III in patients in comparison with controls. Lupus anticoagulant was not found in the patient group and once in the control subjects.
CONCLUSIONS: We conclude that it is unlikely that prothrombotic factors are involved in the pathogenesis of spinal dural arteriovenous fistulas, but subtle associations are not ruled out.Semicarbazide-sensitive amine oxidase in pre-eclampsia: No relation with markers of endothelial cell activationhttp://repub.eur.nl/pub/64316/
Tue, 01 Oct 2002 00:00:01 GMT<div>J.M. Sikkema</div><div>A. Franx</div><div>R. Fijnheer</div><div>P.G.J. Nikkels</div><div>H.W. Bruinse</div><div>F. Boomsma</div>
Background: Semicarbazide sensitive amine-oxidase (SSAO) is an adhesion molecule and thought to play a role in endothelial cell dysfunction (ECD). SSAO has never been associated with markers of ECD. Pre-eclampsia (PE) is, like the early stages of atherosclerosis, characterised by ECD. SSAO could contribute to ECD in PE. Methods: Plasma samples were obtained in 14 pre-eclamptic patients and 14 matched controls. In these SSAO-activity, von Willebrand factor (vWF) levels and ED1 fibronectin levels were determined. Placental tissue was collected of 12 pre-eclamptic pregnancies, 8 preterm deliveries and 12 term controls. In these samples, SSAO activity was assessed. In a subset of these placentas, immunohistochemical staining was performed for SSAO, ICAM-1 and VCAM-1. Results: Plasma SSAO activity was not significantly different between pre-eclamptic subjects and controls. VWF and ED1 fibronectin were both significantly increased in the pre-eclamptic subjects. There was no correlation between SSAO activity and vWF or ED1 fibronectin levels. Placental SSAO activity was not different between pre-eclamptic pregnancies, preterm deliveries and term controls. There was strong staining of SSAO in vascular smooth muscle cells (VSM) and moderate staining of trophoblast in all three groups. Endothelial cell expression of SSAO was only seen in term controls and the placentas of pre-eclamptic patients. There was no association between the expression of SSAO, ICAM-1 or VCAM-1 in the placentas of pre-eclamptic patients. Conclusion: SSAO expression and activity are not related to markers of ECD.